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      Adipokines and inflammation: is it a question of weight? : Obesity and inflammatory diseases

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          Abstract

          <p class="first" id="d3247950e466">Obesity has reached epidemic proportions in the Western society and is increasing in the developing world. It is considered as one of the major contributors to the global burden of disability and chronic diseases, including autoimmune, inflammatory and degenerative diseases. Research conducted on obesity and its complications over the last two decades has transformed the outdated concept of white adipose tissue (WAT) merely serving as an energy depot. WAT is now recognized as an active and inflammatory organ capable of producing a wide variety of factors known as adipokines. These molecules participate through endocrine, paracrine, autocrine or juxtacrine crosstalk mechanisms in a great variety of physiological or pathophysiological processes, regulating food intake, insulin sensitivity, immunity and inflammation. Although initially restricted to metabolic activities (regulation of glucose and lipid metabolism), adipokines currently represent a new family of proteins that can be considered key players in the complex network of soluble mediators involved in the pathophysiology of immune/inflammatory diseases. However, the complexity of the adipokine network in the pathogenesis and progression of inflammatory diseases has posed, since the beginning, the important question of whether it may be possible to target the mechanism(s) by which adipokines contribute to disease selectively without suppressing their physiological functions. Here, we explore in depth the most recent findings concerning the involvement of adipokines in inflammation and immune responses, in particular in rheumatic, inflammatory and degenerative diseases. We also highlight several possible strategies for therapeutic development and propose that adipokines and their signalling pathways may represent innovative therapeutic strategies for inflammatory disorders. </p>

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          Most cited references61

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          Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency

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            Lipocalin-2: A Master Mediator of Intestinal and Metabolic Inflammation.

            Lipocalin-2 (LCN2), also known as neutrophil gelatinase-associated lipocalin (NGAL), is released by various cell types and is an attractive biomarker of inflammation, ischemia, infection, and kidney damage. Both intestinal and metabolic inflammation, as observed in obesity and related disorders, are associated with increased LCN2 synthesis. While LCN2 in the intestinal tract regulates the composition of the gut microbiota and shows anti-inflammatory activities, it also exhibits proinflammatory activities in other experimental settings. In animal models of metabolic inflammation, type 2 diabetes mellitus (T2DM), or nonalcoholic steatohepatitis (NASH), increased LCN2 expression favors inflammation via the recruitment of inflammatory cells, such as neutrophils, and the induction of proinflammatory cytokines. A better understanding of this crucial marker of innate immunity might pave the way for targeting this pathway in future therapies.
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              Is Open Access

              THE CONCISE GUIDE TO PHARMACOLOGY 2017/18: Overview

              The Concise Guide to PHARMACOLOGY 2017/18 is the third in this series of biennial publications. This version provides concise overviews of the key properties of nearly 1800 human drug targets with an emphasis on selective pharmacology (where available), plus links to an open access knowledgebase of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. Although the Concise Guide represents approximately 400 pages, the material presented is substantially reduced compared to information and links presented on the website. It provides a permanent, citable, point‐in‐time record that will survive database updates. The full contents of this section can be found at http://onlinelibrary.wiley.com/doi/10.1111/bph.13882/full. In addition to this overview, in which are identified ‘Other protein targets’ which fall outside of the subsequent categorisation, there are eight areas of focus: G protein‐coupled receptors, ligand‐gated ion channels, voltage‐gated ion channels, other ion channels, nuclear hormone receptors, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The landscape format of the Concise Guide is designed to facilitate comparison of related targets from material contemporary to mid‐2017, and supersedes data presented in the 2015/16 and 2013/14 Concise Guides and previous Guides to Receptors and Channels. It is produced in close conjunction with the Nomenclature Committee of the Union of Basic and Clinical Pharmacology (NC‐IUPHAR), therefore, providing official IUPHAR classification and nomenclature for human drug targets, where appropriate.
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                Author and article information

                Journal
                British Journal of Pharmacology
                British Journal of Pharmacology
                Wiley
                00071188
                May 2018
                May 2018
                April 10 2018
                : 175
                : 10
                : 1569-1579
                Affiliations
                [1 ]SERGAS (Servizo Galego de Saude) and IDIS (Instituto de Investigación Sanitaria de Santiago), The NEIRID Group (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases); Santiago University Clinical Hospital; Building C, Travesía da Choupana S/N Santiago de Compostela 15706 Spain
                [2 ]Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases; Universidad de Cantabria and IDIVAL, Hospital Universitario Marqués de Valdecilla; Av. Valdecilla Santander 39008 Spain
                [3 ]SERGAS (Servizo Galego de Saude), Division of Rheumatology; Santiago University Clinical Hospital; Travesía da Choupana S/N Santiago de Compostela 15706 Spain
                [4 ]SERGAS (Servizo Galego de Saude) and IDIS (Instituto de Investigación Sanitaria de Santiago), Department of Cellular and Molecular Cardiology; CIBERCV (Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares), Building C; Travesía da Choupana S/N Santiago de Compostela 15706 Spain
                [5 ]Musculoskeletal Pathology Group. SERGAS (Servizo Galego de Saude) and IDIS (Instituto de Investigación Sanitaria de Santiago), Research Laboratory 9; Santiago University Clinical Hospital; Santiago de Compostela Spain
                [6 ]Faculty of Health and Medical Sciences; University of Surrey; Guildford Surrey GU2 7XH UK
                [7 ]School of Veterinary Medicine; University of Surrey; Guildford GU2 7AL UK
                [8 ]Arthritis Research UK Centre for Sport, Exercise and Osteoarthritis, Arthritis Research UK Centre for Musculoskeletal Ageing Research; Queen's Medical Centre; Nottingham NG7 2UH UK
                [9 ]State Research Institute Centre for Innovative Medicine; Santariskiu 5 Vilnius 0866 Republic of Lithuania
                Article
                10.1111/bph.14181
                5913397
                29486050
                787ca007-9eaf-4a65-b6e4-6d86cbc36fee
                © 2018

                http://doi.wiley.com/10.1002/tdm_license_1.1

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